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Spontaneous echo contrast in the left atrium during paroxysmal atrial fibrillation
988
Brief Communications
American
t--1200
WA
msec
October 1990 Heart Journal
4
:
l-520 -I msec
t
500
I
msec
2. AV nodal blockade produced with superselectiveinjection of 2 ml of iced saline. The ventricular rate representsventricular pacing at 50 beats/min (cycle length = 1200msec)while the atria are paced at 115beats/min (cycle length = 520 msec).Note continued block below the His with no relationship between the AH and the V intervals. I, II, and III are surface electrocardiogramleads.R VA, Right ventricular apex electrogram; RA, right atria1 electrogram; HBE, His bundle electrogram; Si is the pacing stimulus.
Fig.
attempted.6 This report demonstratesthe potential feasibility of transient or permanent AV nodal blockade using agentssuchasiced salineor ethanol. If permanent ablation is attempted with ethanol or other nonreversible agents, superselectivearterial injection, as describedin this case, will be necessaryto avoid significant myocardial injury. AV nodal artery cannulation, injection, and ablation appearto offer a promisingunique modality with which to treat certain refractory supraventricular arrhythmias. REFERENCES
1. Gallagher JJ, Svenson RH, Kasell JH, et al. Catheter technique for closed-chest ablation of the atrioventricular system. N Engl J Med 1982;306:194-200. 2. Evans GT, Scheinman MM, Fox C, Rodriques M. Predictors of successful His bundle ablation: a report of the percutaneous cardiac mapping and ablation registry [Abstract]. J Am Co11 Cardiol 1988;11:17A. 3. Haissaguerre M, Warin JF, Lemetayer P, Saoudi N, Guillem JP, Blanchot P. Closed-chest ablation of retrograde conduction in patients with atrioventricular nodal reentrant tachycardia. N Engl J Med 1989;320:426-33. 4. Brugada, P, de Swart H, Smeets JLRM, Wellens HJJ. Transcoronary chemical ablation of ventricular tachycardia. Circulation 1989;79:475-82. 5. Wang PJ, Schoen FJ, Reagan K, Hasan HHR, Guo HS, Friedman PL. Modification of atrioventricular conduction by selective atrioventricular nodal artery catheterization. PACE 1990;13:88-102. 6. Freidman, PL, Sosa-Suarez, G, Wang P. Selective AV nodal artery catheterization in humans. Circulation 1989;4(suppl II):II-40.
Spontaneous echo contrast in the left atrium during paroxysmal atrial fibrillation Timothy P. Obarski, DO, Ernest0 E. Salcedo, MD, Lon W. Castle, MD, and William J. Stewart, MD, Cleveland, Ohio
Spontaneousechocontrasts, termed “microcavitations” or “smoke,” have beenseenby transthoracic and transesophagealechocardiographyin the left atrium in patients with mitral valve disease,primarily mitral stenosisor prosthetic mitral valves.’ We describe a patient with paroxysmal atria1 fibrillation who presented with a cerebral embolic stroke and who was found to have spontaneousleft atria1 echo contrast on transesophagealechocardiographywhile in atria1 fibrillation with no evidence of mitral valve disease.To our knowledge,this is the first reported caseof spontaneousleft atrial echo contrast with a normal mitral valve and helps explain the pathophysiology of embolic events in paroxysmal atria1 fibrillation. A 76-year-old man with a history of sick sinussyndrome From the Department of Cardiology, Cleveland Clinic Foundation. Reprint requests: Timothy P. Obarski, DO, Riverside Heart, Inc. 3545 Olentangy River Rd., Columbus, OH 43214. 414122909
Volume Number
120 4
Brief Communications
989
Fica. 1. Transesonhaeealechocardioeranhic view of the left atrium depicting “smoke” or stasisof blood
flow during atrial‘fibryllation. and pacemakerimplantation for symptomatic bradycardia presentedto the emergency room with a stroke. He had a history of paroxysmal atria1fibrillation, which wastreated with verapamil, flecainide, and warfarin anticoagulation. His warfarin wasdiscontinued 2 weeksprior to his referral by his family physician after a Holter monitor had documented normal sinusrhythm. He presentedwith a sudden onset of ataxia, confusion, and dysarthria, along with clumsinessof the right hand and a right hemianopsia.He was dysphasic with normal comprehension,and had significant difficulty with spontaneousverbal output. A computed tomographic scan of the brain wascompatible with a recent infarct in the left posterior cerebral artery distribution. A carotid duplex ultrasound scanwith Doppler revealed minimal plaques in both proximal internal carotid arteries, with a 530% narrowing in each. A transthoracic echocardiogramrevealed a moderately enlargedleft atrium of 4.5 cm with a normal mitral and aortic valve and left ventricular chamber.There wasno cardiac sourceof emboli identified. A transesophagealechocardiogram was performed, which wasunremarkable except for the presenceof left atria1 spontaneousecho contrast or “smoke” diffusely throughout the left atrium. A well-defined thrombus was not visualized. The electrocardiographic (ECG) monitor showedatria1fibrillation with a rapid ventricular response. A continuous ECG recording documented frequent episodesof paroxysmal atria1 fibrillation. One week later after conversion to sinus rhythm, a repeat transesophageal echocardiogram (TEE) was performed, which revealed spontaneous echo contrast localized to the left atria1 appendage. Spontaneousecho contrast consistent with blood stasis can occur in the left atrium during atria1 fibrillation in the absenceof mitral valve diseaseand may help explain the pathophysiology of embolic events in paroxysmal atria1arrhythmias. At the time of the initial TEE, the patient was in atria1 fibrillation and the left atrium wasdiffusely filled
with spontaneousechocontrast (Fig. 1). A repeat TEE with the patient in sinus rhythm revealed the body of the left atrium to be free of spontaneousechoes,suggestiveof improved blood flow; however, evidence of blood stasis remained in the left atria1 appendage(Fig. 2). This residual localization of blood stasiscould explain the high incidenceof embolic events in the first few days after conversion to sinusrhythm.2 Whether this blood stasisimproves over time, provided sinusrhythm is maintained, needsto be determined. The incidenceof spontaneousleft atria1 echocontrast on transthoracic echo is 0.1%.3 These patients all had aneurysmal dilation of the left atrium due to mitral valve disease.The incidence in mitral valve diseaseranges from 31% on transthoracic echocardiograph to 50% by TEE.5 In the latter study, there was a significant correlation between the presence of spontaneous echoes, left atria1 thrombi, and peripheral embolic events. In our review of patients with symptomatic mitral stenosis, spontaneous echoes in the left atrium significantly correlated with severity of mitral valve narrowing (p = 0.003) and the presenceof atria1 fibrillation (p = 0.001). Systemic emboli were 2.6 times more frequent in the patients with spontaneousechoes(unpublished data). These observationssuggestthat patients with paroxysmal atria1 fibrillation and a normal mitral valve should be consideredfor systemicanticoagulation if no contraindications exist. REFERENCES
1. Iliceto S, Antonelli G, Sorino M, Biasco G, Rizzon P. Dynamic intracavitary left atria1 echoes in mitral stenosis. Am J Cardiol 1985;55:603-6. 2. Sherman DG, Goldman L, Lohiting RB, Jungensen K, Kaste M, Easton JD. Thromboembolism in patients with atria1 fibrillation. Arch Neurol 1984;41:708. 3. Garcia Fernandez MA, Moreno M, Banuelos F. Two-dimensional echocardiographic identification of blood stasis in the left atrium. AM HEARTJ 1985;109:600-1.
990
Brief Communications
American
October 1990 Heart Journal
Fig. 2. Transesophagealechocardiographicview of the samepatient as in Fig. 1 in sinus rhythm. The “smoke” is now localized to the left atria1 appendage.
4. Beppu S, Nimura Y, Sakakibara H, Nagata S, Park YD, Izumi S. Smoke-like echo in the left atrial cavity in mitral valve disease: its features and significance. J Am Co11 Cardiol 1985;6:744-9. 5. Daniel WG, Nellessen U, Schroder E, Nonnast-Daniel B, Bednarski P, Nikutta P, Lichtlen PR. Left atria1 spontaneous echo contrast in mitral valve disease. An indicator for an increased thromboembolic risk. J Am Co11Cardiol1988;11:120411.
Left ventricular pseudoaneurysm: Detection and postoperative follow-up color Doppler echocardiography
by
Benjamin Rueda, MD, Ioannis P. Panidis, MD, Ray Gonzales, and Michael McDonough, MD. Philadelphia,
Pa.
Ventricular rupture following myocardial infarction results in hemopericardium with cardiac tamponade and is invariably fatal unless surgical intervention is urgently undertaken. Rarely, adherent parietal pericardium confines the myocardial rupture and creates a pseudoaneurysm or falseaneurysm,a large thin-walled sacwith a small narrow-necked orifice communicatingwith the left ventricle. Spontaneousrupture of pseudoaneurysms,however, is a well-recognized complication, sothat early and accurate diagnosisis essentialbecausethis condition is amenableto surgical cure.le3Two-dimensional and Doppler echocarFrom the Division sity Hospital. Reprint University 414122684
of Cardiology,
Department
requests: Ioannis P. Panidis, Hospital, 3401 N. Broad
of Medicine,
MD, Section St., Philadelphia,
Temple
Univer-
of Cardiology, PA 19140.
Temple
diography have been very helpful in the detection of pseudoaneurysms.4-8 We describea patient with a pseudoaneurysmcharacterized by multiple communicationswith the posterior left ventricular wall clearly demonstrated by color-flow Doppler echocardiography and postoperative residual flow disturbance at the site of repair, that eventually resolved 2 months after surgery. A 64-year-old man with coronary artery bypasssurgery 9 years before was admitted with an acute anterior wall myocardial infarction. He had sustained an inferior wall infarction 3 months previously. On admission,there were no clinical signsof heart failure; a grade 2/6 holosystolic murmur was heard at the apex. On the chest roentgenogramlung fieldswerenormal and cardiomegalywaspresent. Electrocardiogram revealed an evolving acute anterior wall myocardial infarction and a previous inferior infarct. Coronary arteriography showednear-total occlusionof the left main coronary artery, patent saphenousvein graft to the diagonal branch, and a 90% distal lesion in the saphenous vein graft to the left anterior descendingartery. The left circumflex artery wastotally occludedafter the first obtuse marginal branch. A radionuclide ventriculogram demonstrated an inferoposterior accessorychambercommunicating with the left ventricle. Two-dimensional echocardiography revealed akinesis of the distal septum and apex, severehypokinesisof the inferior wall, and an apical laminated thrombus. A large inferoposterior saccularchamber wasvisualized, communicatingwith multiple orifices with the left ventricle (Fig. 1, A, top). Bidirectional phasicflow into and out of the pseudoaneurysmwas confirmed by pulsedDoppler echocardiography,and two distinct systolic jets wereclearly visualized by color-flow Doppler mapping (Fig. 1, A, bottom). Mild mitral regurgitation waspresent. At surgery, six communicationsbetween the pseudoaneurysm and the left ventricle werefound and were closedwith pledget-supported horizontal mattress sutures. The pseudoaneurysmitself wasplicated and wasreclosedin an
Brief Communications
American
t--1200
WA
msec
October 1990 Heart Journal
4
:
l-520 -I msec
t
500
I
msec
2. AV nodal blockade produced with superselectiveinjection of 2 ml of iced saline. The ventricular rate representsventricular pacing at 50 beats/min (cycle length = 1200msec)while the atria are paced at 115beats/min (cycle length = 520 msec).Note continued block below the His with no relationship between the AH and the V intervals. I, II, and III are surface electrocardiogramleads.R VA, Right ventricular apex electrogram; RA, right atria1 electrogram; HBE, His bundle electrogram; Si is the pacing stimulus.
Fig.
attempted.6 This report demonstratesthe potential feasibility of transient or permanent AV nodal blockade using agentssuchasiced salineor ethanol. If permanent ablation is attempted with ethanol or other nonreversible agents, superselectivearterial injection, as describedin this case, will be necessaryto avoid significant myocardial injury. AV nodal artery cannulation, injection, and ablation appearto offer a promisingunique modality with which to treat certain refractory supraventricular arrhythmias. REFERENCES
1. Gallagher JJ, Svenson RH, Kasell JH, et al. Catheter technique for closed-chest ablation of the atrioventricular system. N Engl J Med 1982;306:194-200. 2. Evans GT, Scheinman MM, Fox C, Rodriques M. Predictors of successful His bundle ablation: a report of the percutaneous cardiac mapping and ablation registry [Abstract]. J Am Co11 Cardiol 1988;11:17A. 3. Haissaguerre M, Warin JF, Lemetayer P, Saoudi N, Guillem JP, Blanchot P. Closed-chest ablation of retrograde conduction in patients with atrioventricular nodal reentrant tachycardia. N Engl J Med 1989;320:426-33. 4. Brugada, P, de Swart H, Smeets JLRM, Wellens HJJ. Transcoronary chemical ablation of ventricular tachycardia. Circulation 1989;79:475-82. 5. Wang PJ, Schoen FJ, Reagan K, Hasan HHR, Guo HS, Friedman PL. Modification of atrioventricular conduction by selective atrioventricular nodal artery catheterization. PACE 1990;13:88-102. 6. Freidman, PL, Sosa-Suarez, G, Wang P. Selective AV nodal artery catheterization in humans. Circulation 1989;4(suppl II):II-40.
Spontaneous echo contrast in the left atrium during paroxysmal atrial fibrillation Timothy P. Obarski, DO, Ernest0 E. Salcedo, MD, Lon W. Castle, MD, and William J. Stewart, MD, Cleveland, Ohio
Spontaneousechocontrasts, termed “microcavitations” or “smoke,” have beenseenby transthoracic and transesophagealechocardiographyin the left atrium in patients with mitral valve disease,primarily mitral stenosisor prosthetic mitral valves.’ We describe a patient with paroxysmal atria1 fibrillation who presented with a cerebral embolic stroke and who was found to have spontaneousleft atria1 echo contrast on transesophagealechocardiographywhile in atria1 fibrillation with no evidence of mitral valve disease.To our knowledge,this is the first reported caseof spontaneousleft atrial echo contrast with a normal mitral valve and helps explain the pathophysiology of embolic events in paroxysmal atria1 fibrillation. A 76-year-old man with a history of sick sinussyndrome From the Department of Cardiology, Cleveland Clinic Foundation. Reprint requests: Timothy P. Obarski, DO, Riverside Heart, Inc. 3545 Olentangy River Rd., Columbus, OH 43214. 414122909
Volume Number
120 4
Brief Communications
989
Fica. 1. Transesonhaeealechocardioeranhic view of the left atrium depicting “smoke” or stasisof blood
flow during atrial‘fibryllation. and pacemakerimplantation for symptomatic bradycardia presentedto the emergency room with a stroke. He had a history of paroxysmal atria1fibrillation, which wastreated with verapamil, flecainide, and warfarin anticoagulation. His warfarin wasdiscontinued 2 weeksprior to his referral by his family physician after a Holter monitor had documented normal sinusrhythm. He presentedwith a sudden onset of ataxia, confusion, and dysarthria, along with clumsinessof the right hand and a right hemianopsia.He was dysphasic with normal comprehension,and had significant difficulty with spontaneousverbal output. A computed tomographic scan of the brain wascompatible with a recent infarct in the left posterior cerebral artery distribution. A carotid duplex ultrasound scanwith Doppler revealed minimal plaques in both proximal internal carotid arteries, with a 530% narrowing in each. A transthoracic echocardiogramrevealed a moderately enlargedleft atrium of 4.5 cm with a normal mitral and aortic valve and left ventricular chamber.There wasno cardiac sourceof emboli identified. A transesophagealechocardiogram was performed, which wasunremarkable except for the presenceof left atria1 spontaneousecho contrast or “smoke” diffusely throughout the left atrium. A well-defined thrombus was not visualized. The electrocardiographic (ECG) monitor showedatria1fibrillation with a rapid ventricular response. A continuous ECG recording documented frequent episodesof paroxysmal atria1 fibrillation. One week later after conversion to sinus rhythm, a repeat transesophageal echocardiogram (TEE) was performed, which revealed spontaneous echo contrast localized to the left atria1 appendage. Spontaneousecho contrast consistent with blood stasis can occur in the left atrium during atria1 fibrillation in the absenceof mitral valve diseaseand may help explain the pathophysiology of embolic events in paroxysmal atria1arrhythmias. At the time of the initial TEE, the patient was in atria1 fibrillation and the left atrium wasdiffusely filled
with spontaneousechocontrast (Fig. 1). A repeat TEE with the patient in sinus rhythm revealed the body of the left atrium to be free of spontaneousechoes,suggestiveof improved blood flow; however, evidence of blood stasis remained in the left atria1 appendage(Fig. 2). This residual localization of blood stasiscould explain the high incidenceof embolic events in the first few days after conversion to sinusrhythm.2 Whether this blood stasisimproves over time, provided sinusrhythm is maintained, needsto be determined. The incidenceof spontaneousleft atria1 echocontrast on transthoracic echo is 0.1%.3 These patients all had aneurysmal dilation of the left atrium due to mitral valve disease.The incidence in mitral valve diseaseranges from 31% on transthoracic echocardiograph to 50% by TEE.5 In the latter study, there was a significant correlation between the presence of spontaneous echoes, left atria1 thrombi, and peripheral embolic events. In our review of patients with symptomatic mitral stenosis, spontaneous echoes in the left atrium significantly correlated with severity of mitral valve narrowing (p = 0.003) and the presenceof atria1 fibrillation (p = 0.001). Systemic emboli were 2.6 times more frequent in the patients with spontaneousechoes(unpublished data). These observationssuggestthat patients with paroxysmal atria1 fibrillation and a normal mitral valve should be consideredfor systemicanticoagulation if no contraindications exist. REFERENCES
1. Iliceto S, Antonelli G, Sorino M, Biasco G, Rizzon P. Dynamic intracavitary left atria1 echoes in mitral stenosis. Am J Cardiol 1985;55:603-6. 2. Sherman DG, Goldman L, Lohiting RB, Jungensen K, Kaste M, Easton JD. Thromboembolism in patients with atria1 fibrillation. Arch Neurol 1984;41:708. 3. Garcia Fernandez MA, Moreno M, Banuelos F. Two-dimensional echocardiographic identification of blood stasis in the left atrium. AM HEARTJ 1985;109:600-1.
990
Brief Communications
American
October 1990 Heart Journal
Fig. 2. Transesophagealechocardiographicview of the samepatient as in Fig. 1 in sinus rhythm. The “smoke” is now localized to the left atria1 appendage.
4. Beppu S, Nimura Y, Sakakibara H, Nagata S, Park YD, Izumi S. Smoke-like echo in the left atrial cavity in mitral valve disease: its features and significance. J Am Co11 Cardiol 1985;6:744-9. 5. Daniel WG, Nellessen U, Schroder E, Nonnast-Daniel B, Bednarski P, Nikutta P, Lichtlen PR. Left atria1 spontaneous echo contrast in mitral valve disease. An indicator for an increased thromboembolic risk. J Am Co11Cardiol1988;11:120411.
Left ventricular pseudoaneurysm: Detection and postoperative follow-up color Doppler echocardiography
by
Benjamin Rueda, MD, Ioannis P. Panidis, MD, Ray Gonzales, and Michael McDonough, MD. Philadelphia,
Pa.
Ventricular rupture following myocardial infarction results in hemopericardium with cardiac tamponade and is invariably fatal unless surgical intervention is urgently undertaken. Rarely, adherent parietal pericardium confines the myocardial rupture and creates a pseudoaneurysm or falseaneurysm,a large thin-walled sacwith a small narrow-necked orifice communicatingwith the left ventricle. Spontaneousrupture of pseudoaneurysms,however, is a well-recognized complication, sothat early and accurate diagnosisis essentialbecausethis condition is amenableto surgical cure.le3Two-dimensional and Doppler echocarFrom the Division sity Hospital. Reprint University 414122684
of Cardiology,
Department
requests: Ioannis P. Panidis, Hospital, 3401 N. Broad
of Medicine,
MD, Section St., Philadelphia,
Temple
Univer-
of Cardiology, PA 19140.
Temple
diography have been very helpful in the detection of pseudoaneurysms.4-8 We describea patient with a pseudoaneurysmcharacterized by multiple communicationswith the posterior left ventricular wall clearly demonstrated by color-flow Doppler echocardiography and postoperative residual flow disturbance at the site of repair, that eventually resolved 2 months after surgery. A 64-year-old man with coronary artery bypasssurgery 9 years before was admitted with an acute anterior wall myocardial infarction. He had sustained an inferior wall infarction 3 months previously. On admission,there were no clinical signsof heart failure; a grade 2/6 holosystolic murmur was heard at the apex. On the chest roentgenogramlung fieldswerenormal and cardiomegalywaspresent. Electrocardiogram revealed an evolving acute anterior wall myocardial infarction and a previous inferior infarct. Coronary arteriography showednear-total occlusionof the left main coronary artery, patent saphenousvein graft to the diagonal branch, and a 90% distal lesion in the saphenous vein graft to the left anterior descendingartery. The left circumflex artery wastotally occludedafter the first obtuse marginal branch. A radionuclide ventriculogram demonstrated an inferoposterior accessorychambercommunicating with the left ventricle. Two-dimensional echocardiography revealed akinesis of the distal septum and apex, severehypokinesisof the inferior wall, and an apical laminated thrombus. A large inferoposterior saccularchamber wasvisualized, communicatingwith multiple orifices with the left ventricle (Fig. 1, A, top). Bidirectional phasicflow into and out of the pseudoaneurysmwas confirmed by pulsedDoppler echocardiography,and two distinct systolic jets wereclearly visualized by color-flow Doppler mapping (Fig. 1, A, bottom). Mild mitral regurgitation waspresent. At surgery, six communicationsbetween the pseudoaneurysm and the left ventricle werefound and were closedwith pledget-supported horizontal mattress sutures. The pseudoaneurysmitself wasplicated and wasreclosedin an